doi 10.1308/147870810X12659688851915
On-line Case Report
Transmural eosinophilic gastritis with gastric outlet obstruction: case report and review of the literature DAVID J HOLROYD1, SASWATA BANERJEE1, KHURRAM S CHAUDHARY2, SOPHIE RESHAMWALLA1, VARDHINI VIJAY1, MICHAEL W WARD1 Departments of 1General Surgery and 2Cellular Pathology, Barnet and Chase Farm Hospitals NHS Trust, Enfield, UK
ABSTRACT Eosinophil-associated gastrointestinal disorders (EGIDs) are uncommon conditions whose aetiologies are unclear, but which are characterised by eosinophilic infiltration and inflammation of the gastrointestinal tract in the absence of other causes of eosinophilia. We report the case of a 65-year-old woman with eosinophilic gastritis who underwent a Polya gastrectomy for a suspected gastric tumour with gastric outflow obstruction. Subsequent histological examination showed a non-malignant transmural eosinophilic infiltration of the stomach wall, a rare pathological entity. We present a review of the literature and discuss the management of such cases. Keywords: Eosinophilic gastritis – Transmural eosinophilic infiltration – EGIDs
Case history
A 65-year-old woman was referred with a 2-month
history of epigastric pain, anorexia, early satiety and 5-kg weight loss. There was no history of vomiting or change in bowel habit. She was a life-long non-smoker and significant past medical history included a duodenal ulcer, for which she was taking ranitidine. She had also been recently diagnosed with Graves’ thyrotoxicosis and had been started on carbimazole, although she continued to lose weight after starting treatment and was biochemically euthyroid. On examination, a firm, non-tender 5 × 5 cm mobile mass was palpable in the epigastrium. There was no cervical lymphadenopathy, hepatosplenomegaly or ascites. Routine blood tests were normal. Abdominal computed
tomography (CT) displayed a thick-walled and poorly distensible gastric antrum with a small low attenuation lesion seen in the greater curve of the stomach (Fig. 1A) and several adjacent lymph nodes (Fig. 1B). A subsequent oesphagogastroduodenoscopy was entirely normal with no obvious gastric mass or ulceration. No biopsies were taken. A limited colonoscopy to the mid transverse colon was also unremarkable. The patient developed symptoms of gastric outlet obstruction and an expedited laparotomy was performed. A mass was found arising from the greater curvature of the stomach, infiltrating the transverse mesocolon. A Polya partial gastrectomy with gastrojejunostomy was performed with resection of adjacent lymph nodes and en-bloc excision of the affected section of transverse colon and mesocolon. The patient had an uneventful postoperative recovery.
Correspondence to: David Holroyd, Department of General Surgery, Barnet & Chase Farm NHS Trust, The Ridgeway, Enfield, London EN2 8JL, UK E:
[email protected] Ann R Coll Surg Engl 2010; 92
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HOLROYD, BANERJEE, CHAUDHARY, RESHAMWALLA, VIJAY, WARD
Transmural eosinophilic gastritis with gastric outlet obstruction
A
B
C
D
Figure 1 (A) CT image showing a small focal low attenuation lesion seen in the greater curve of the stomach. (B) CT image showing several small lymph nodes adjacent to the stomach. (C) Photomicrograph highlighting transmural nature of the inflammatory process with numerous eosinophils within the muscularis propria of the stomach. (D) Histological features of eosinophilic vasculitis with infiltration of eosinophils within the wall of a medium-sized vein.
Macroscopic examination of the partial gastrectomy specimen showed generalised thickening of the gastric wall with an indurated serosal surface and area of mucosal ulceration. Microscopic examination revealed complete mucosal loss at the large ulcer site with widespread fibrosis replacing much of the lamina propria and a transmural inflammatory infiltrate composed predominantly of eosinophils. Features of eosinphilic vasculitis were also seen. Multiple lymph nodes showed reactive changes only. Helicobacter pylori organisms were not identified and there was no evidence of carcinoma. The patient was on a 6-monthly follow-up pathway, when she re-presented 2 years later with vomiting and upper abdominal pain. On clinical examination, a hard, non-tender mass was again palpable, this time in the right upper quadrant. A CT scan showed a grossly thickened gall-bladder wall with no biliary dilatation or lymphadenopathy. The possibility of eosinophilic cholecystitis was considered along with carcinoma of the gall-bladder. She was referred to a tertiary centre and underwent a radical cholecystectomy. Histology of the gall-bladder showed inflammation consistent with cholecystitis but no evidence of malignancy. Some eosinophil prominence was evident, although not as marked infiltration seen in the gastrectomy specimen. The patient made an uneventful recovery and remains well 3 months later. 2
Discussion Eosinophil-associated gastrointestinal disorders (EGIDs) are relatively rare heterogeneous conditions that affect the GI tract and are characterised by eosinophil-rich inflammation. The aetiology of EGIDs is unknown and elevated eosinophil counts are seen in approximately 75% of cases. EGIDs can be classified according to location and the layer(s) of the gastrointestinal tract involved. Clinical symptoms also vary according to the site, layer and depth of gastrointestinal wall involved. Three criteria are used in the diagnosis of EGIDs: (i) the presence of gastrointestinal symptoms; (ii) biopsies showing eosinophilic infiltration of one or more areas of the gastrointestinal tract (> 20 eosinophils per high power field) or typical radiological findings with a peripheral eosinophilia; and (iii) no evidence of extra-intestinal disease or parasitic disease.1 Eosinophilic gastritis (EG) affects the stomach and is one of a number of disorders that collectively form EGIDs. Previous studies have demonstrated that mucosal involvement is the commonest type, seen in approximately 60% of those affected. Muscular involvement is seen in around 30% with subserosal involvement in approximately 10%.1 We believe that this is the first published case in which there has been Ann R Coll Surg Engl 2010; 92
Transmural eosinophilic gastritis with gastric outlet obstruction
HOLROYD, BANERJEE, CHAUDHARY, RESHAMWALLA, VIJAY, WARD
transmural eosinophil infiltration, affecting all layers of the gut wall; an entity which has not been described before and the significance of which is unknown. EG is a rare cause of gastric outflow obstruction, which typically occurs when the muscularis layer is affected2 and may mimic malignancy.3 Intussusception may also occur with muscular disease involving the bowel. In comparison, symptoms seen with the mucosal variety typically include malabsorption and bleeding due to ulceration.1 Such ulceration is often resistant to treatment with proton-pump inhibitors. Occasionally, EGIDs can present with acute abdominal pain, usually as a result of ulceration or obstruction. The endoscopic appearance of eosinophilic gastritis is non-specific, but may include erythematous or ulcerative mucosal changes. Loss of villi may also be apparent, especially when multiple layers are involved. In cases in which no mucosal infiltration is present or infiltration is patchy, endoscopic biopsies may be negative.4 Laparoscopic, full-thickness biopsies can be attempted if endoscopic biopsies prove inconclusive. Eosinophilic cholecystitis is rare with few case reports of the condition since it was first described in 1949. It may occur in isolation or in association with EGIDs. Presentation is usually similar to cholecystitis and, like EGIDs, it may mimic malignancy.5 Surgical management of proven EG is usually reserved for cases in which there is evidence of obstruction.2 EG, however, may simulate gastric carcinoma and diagnosis may only follow radical resection.3 Medical therapy is the main method of treatment of EGIDs and involves
systemic corticosteroids, which suppress cytokine gene transcription and local inflammation. However, symptoms may recur once steroid therapy is stopped and long-term treatment may be required. Sodium cromoglycate and monteleukast may also be effective and targeted immunotherapeutic treatments, including antiIgE and anti-IL-5 may have a future role in the treatment of EGIDs.
Ann R Coll Surg Engl 2010; 92
Conclusions
Diagnosis of eosinophilic gastritis in the context of a possible gastric malignancy may, in the absence of obstruction, avoid surgical intervention and subsequent morbidity as medical treatment is often effective. As in this case, endoscopic biopsies may be inconclusive and the diagnosis made postoperatively. The significance of transmural eosinophilic gastritis is unknown. References
1. Talley NJ, Shorter RG, Phillips SF, Zinmeister AR. Eosinophilic gastroenteritis: a clinicopathological study of patients with disease of the mucosa, muscle layer, and subserosal tissues. Gut 1990; 31: 54–8. 2. Mohammed AA, Benmousa A, Almeghaiseeb I, Alkarawi M. Gastric outlet obstruction. Hepatogastroenterology 2007; 54: 2415–20. 3. Milman PJ, Sidhu GS. Case report: eosinophilic gastritis simulating a neoplasm. Am J Med Sci 1978; 276 :227–30. 4. Yantiss RK, Odze RD. Optimal approach to obtaining mucosal biopsies for assessment of inflammatory disorders of the gastrointestinal tract. Am J Gastroenterol 2009; 104: 774–8. 5. Dabbs DJ. Eosinophilic and lymphoeosinophilic cholecystitis. Am J Surg Pathol 1993; 17: 497–501.
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